Selenium deficiency is functionally linked with the molecular etiopathogenesis of necrotizing enterocolitis (NEC).

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Gürünlüoğlu K., Dündar M., Ünver T., Turgut H., Gürünlüoğlu S., Akpınar N., ...Daha Fazla

Functional & integrative genomics, cilt.25, sa.1, ss.118, 2025 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 25 Sayı: 1
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1007/s10142-025-01628-8
  • Dergi Adı: Functional & integrative genomics
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.118
  • Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
  • İnönü Üniversitesi Adresli: Evet

Özet

Abstract

Necrotizing enterocolitis (NEC) is a severe and often catastrophic gastrointestinal emergency that predominantly affects

neonates, especially those born prematurely, and is associated with high rates of morbidity and mortality. Despite its significant

clinical impact, the precise etiology and molecular pathogenesis of NEC remain incompletely understood. In this study,

we conducted global transcriptomic profiling using high-throughput RNA sequencing in 11 premature neonates diagnosed

with NEC, following rigorous inclusion and exclusion criteria. Compared to healthy controls, we identified 1,204 differentially

expressed genes (DEGs), including 636 upregulated and 568 downregulated transcripts. Notably, genes involved

in hypoxia-induced apoptosis (e.g., HIF1 AAS3, HIF1 AAS1), the caspase cascade (BCL2, BCL6, CASP5, CASP7), and

inflammation (IL1RAP, IL6ST, TNFAIP3, TNFRSF10 A, TLR6, TLR10) were significantly upregulated. In contrast, IL18, a

key modulator of inflammatory responses, was downregulated. Interestingly, several genes encoding selenoproteins (GPX1,

GPX4, SELENON, SELENOM, SELENOF, SELENOW, SELENOT) were also downregulated, suggesting molecular evidence

of selenium deficiency. Gene ontology and pathway enrichment analyses revealed widespread dysregulation in pathways

related to hypoxia response, systemic inflammation, coagulation, antimicrobial defense, mitochondrial function, autophagy,

selenium metabolism, and apoptosis. Collectively, our findings provide novel insights into the molecular underpinnings of

NEC in premature infants and suggest that systemic hypoxia, oxidative stress, selenium deficiency, and programmed cell

death contribute significantly to its pathogenesis.